En Gast 01B PDF

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Common Symptoms and

Signs in Gastroenterology
C. Dubé
With sections authored by:

R.F. Bursey, M.C. Champion, J.M. Fardy, S. Grégoire,
D.G. MacIntosh, D.G. Patel, A. Rostom, N. Saloojee,
L.J. Scully, A.S.C. Sekar, W.G. Thompson and
J.M. Watters
1. INTRODUCTION / W.G. Thompson and C. Dubé
The key to accurate diagnosis and effective management of gastrointestinal

problems is flawless history-taking. Since up to 50% of gastrointestinal disor-
ders are associated with no anatomical change, no physical findings and no
positive test result, diagnosis and therapy must often be based on the medical
interview. The gastrointestinal history must include an accurate description
of the symptom itself, of its relationship with food ingestion and defecation,
a personal and familial history of gastrointestinal disorders, treatment or
surgery and a meticulous search for symptoms that might suggest organic dis-
ease. Finally, the physician should assess the patient’s psychosocial state, with
particular attention directed toward traumatic events or concerns associated
with the onset of his or her complaints.
The physician should determine the time of onset of the symptom, its
occurrence in the past, its periodicity, its location and radiation if appropriate,
its aggravating and relieving factors, and its relationship to dietary as well as
other symptoms. A review of past history should include not only any previ-
ous gastrointestinal surgery or diseases, but also systemic illnesses (such as
diabetes or severe cardiovascular disease) that might affect the gut. One
should pay particular attention to “alarm” symptoms such as gastrointestinal
hemorrhage, profound weight loss, voluminous diarrhea or episodes of
extreme abdominal pain, which might indicate organic disease. Similarly,
4 FIRST PRINCIPLES OF GASTROENTEROLOGY
such phenomena as anemia, fever or incapacity to work may indicate a more

serious gastrointestinal disorder demanding investigation, treatment and fol-
low-up. A family history of peptic ulcer disease, gastric or colonic cancer,
celiac disease, or liver disease may provide clues to the diagnosis as well as
indicate the need to screen for such entities as H. pylori infection, celiac dis-
ease, colonic neoplasm or hemochromatosis
When considering a gastrointestinal complaint, the astute physician cannot
ignore the patient’s psyche. Many studies establish that those who bring
gastrointestinal complaints to a physician, even if they are organic in nature,
frequently have psychosocial disabilities. Failure to identify and manage the
patient’s reaction to his or her psychosocial environment (whether it be hostil-
ity toward a spouse, an abnormal fear of cancer or a profound loss) may lead
to an unsatisfactory therapeutic outcome.
The following is a synopsis of the common gastrointestinal symptoms.
These notes include a description of the symptom itself, a word about how the
symptom is generated, the important historical features and associated physi-
cal findings, and a brief approach to diagnosis and management. These serve
as introductory comments; greater detail can be found throughout the text in
discussions of specific diseases. The final section of this chapter presents a
sequential approach to the examination of the abdomen.
2. GLOBUS / C. Dubé and W.G. Thompson
2.1 Synonyms
Globus hystericus; globus pharyngeus; lump in the throat.
2.2 Description
Globus sensation is defined as the persistent or intermittent sensation of a
lump or foreign body in the throat. This symptom is not associated with food
intake: patients with globus can usually swallow meals normally but feel an
inability to swallow their saliva between meals.
2.3 Epidemiology
Globus sensation is found to occur at least once in up to half of the general
population, usually during an emotional event.
2.4 Etiology
The etiology of globus is unknown but it has been associated with stress,
psychologic and psychiatric disorders; an association with either upper
esophageal sphincter dysfunction, esophageal dysmotility and gastroesophageal
reflux disease has also been suggested, although inconsistently observed.
Common Symptoms and Signs 5
2.5 Differential Diagnosis and Management

It is important to distinguish globus sensation from dysphagia or odynopha-
gia by careful history-taking. Investigations of patients with globus should
be geared at ruling out a pathology of the ear, nose and throat (ENT) spherules
(e.g., oropharyngeal carcinoma), pathologic gastroesophageal reflux or
esophageal motility disorder, especially achalasia. In this regard, a complete
physical and otolaryngological examination should be performed, as well as a
barium swallow with a solid bolus (such as bread or a barium tablet) to
exclude a mechanical problem and to look for an obvious, underlying motility
disorder. Once confirmed by the absence of any organic pathology, globus
sensation is best managed by simple reassurance.
2.6 Management
There is no treatment beyond reassurance. No diagnostic tests are indicated. If
deep-seated emotional features exist, they may warrant a psychiatric opinion.
3. HEARTBURN AND REGURGITATION / C. Dubé and W.G. Thompson
3.1 Description
Heartburn is a burning sensation experienced behind the sternum, which may
radiate toward the neck. It is most commonly experienced in the postprandial
period, or when the subject is bending over, lying down or straining. Unlike
angina, it is not usually worsened by exercise.
Regurgitation is the effortless return of gastric or esophageal contents
into the pharynx without nausea, retching, or abdominal contractions.
Patients typically regurgitate acidic material mixed with small amounts of
undigested food.
Heartburn and regurgitation often occur concomitantly and may also be
associated with chest pain, waterbrash, globus sensation, odynophagia, and
nausea. Waterbrash is defined as the spontaneous flooding of the mouth with
a clear, slightly salty fluid, which may be of sufficient quantity to require
expectoration. It is believed to result from a vagal cholinergic reflex, with
afferences originating in the upper gastrointestinal tract and efferences des-
tined to the salivary glands.
3.2 Epidemiology
Heartburn and/or acid regurgitation is common and occurs at least weekly in
up to 20% of the general population; only a minority of heartburn sufferers
will eventually consult a physician for such symptoms, and those that seek
medical advice may be characterized by a higher anxiety level, recent death or
morbidity in the family as well as associated chronic MSK complaints or pain.
3.3 History
When heartburn is suspected, one should determine the effect of position, food,
stress and exercise on the symptom. A careful cardiac history should be taken
to rule out the possibility of angina. It is important to inquire about dysphagia,
odynophagia, weight loss, symptoms suggestive of bleeding or anemia, as well
as chronic cough or respiratory symptoms that could suggest aspiration.
The presence of heartburn and regurgitation implies that the subject has
gastroesophageal reflux disease (GERD). The approach to investigation and
management of GERD will be reviewed in its designated chapter.
4. DYSPHAGIA / A.S.C. Sekar
4.1 Description
Dysphagia means difficulty in swallowing. Some patients describe food stick-
ing in the throat or retrosternally.
4.2 Important Historical Points and Differential Diagnosis

A careful history is important. Mechanical narrowing is a common cause;
an inflammatory stricture must be distinguished from a carcinoma. If the dys-
phagia is relatively short in duration (e.g., only a few months) and is worsen-
ing, this suggests a progressive mechanical narrowing of the lumen such as
may occur with an esophageal carcinoma. With benign disease, symptoms are
often present for a longer period of time than with carcinoma. A previous his-
tory of heartburn or acid regurgitation in a patient with progressive dysphagia
might point to an esophageal stricture secondary to gastroesophageal reflux
disease. Not all patients with a benign esophageal stricture have a clear histo-
ry of preceding heartburn or acid regurgitation. This is particularly true in the
elderly patient. A history of ingestion of caustic agents such as lye suggests
an esophageal stricture secondary to severe chemical esophagitis.
Infections of the esophagus can also cause difficult swallowing. Infections,
usually due to Candida albicans or herpes virus, are often accompanied by sig-
nificant pain on swallowing, termed odynophagia. Often the odynophagia is so
severe that the patient even has difficulty swallowing his or her saliva. Although
herpes esophagitis can occur in relatively healthy patients, Candida esophagitis
is associated with diabetes, an underlying malignancy or immunosuppression.
The patient may point to the site of obstruction, but this is not always reli-
able. A stricture of the lower esophagus may be experienced at the xiphoid
area or as high as the throat. Upper esophageal obstruction is experienced high
in the throat region, not low in the chest.
Dysphagia can also occur with motor disorders of the esophagus. These con-
ditions include esophageal spasm and achalasia. With motor disorders of the
esophagus, the dysphagia may be for both solids and liquids. The dysphagia is
intermittent and may have a long history. Sometimes with esophageal spasm the
dysphagia may be accompanied by pain (odynophagia), especially with extremely
cold or hot liquids. These patients are usually able to wash down impacted
particles of food, whereas patients with a mechanical cause (such as a stricture)
may need to regurgitate impacted particles of food to obtain relief.
A common cause of intermittent dysphagia is a mucosal ring at the gastro-
esophageal junction (lower esophageal or Schatzki’s ring). On occasion when
a relatively large bolus of food is swallowed the ring can cause mechanical
obstruction, producing a dramatic onset of acute dysphagia (sometimes asso-
ciated with pain). Often such patients will have to leave the table and regurgi-
tate. Patients with a Schatzki’s ring usually have symptoms for many years
before they seek medical attention.
A rare cause of upper esophageal dysphagia is the Paterson-Kelly syn-
drome or Plummer-Vinson syndrome. Here, a chronic iron deficiency anemia
is associated with narrowing of the upper esophagus due to a web.
Cricopharyngeal dysphagia may be due to a cricopharyngeal or Zenker’s
diverticulum, which develops from an abnormality of the cricopharyngeal
sphincter. Patients with a diverticulum often complain of regurgitating food
that they swallowed a day or so earlier.
There are non-esophageal causes of dysphagia. Underlying neuromuscular
disease may cause cricopharyngeal dysphagia, where patients have difficulty
initiating a swallow. A large goiter or mediastinal tumor can cause extrinsic
compression of the upper esophagus.
4.3 Approach to Diagnosis and Management

A barium swallow is the most important initial investigation in the diagnosis of
dysphagia. It might reveal a Zenker’s diverticulum, an esophageal stricture
(benign or malignant) or a Schatzki’s ring. If inflammation of the esophagus is
suspected, endoscopy with biopsies is indicated. If a stricture is identified on a
barium swallow, endoscopy with biopsies is necessary to determine whether this
stricture is benign or malignant. Also, benign strictures can be dilated following
the endoscopic diagnosis. A barium swallow may help diagnose motility distur-
bances such as esophageal spasm and achalasia. Esophageal manometry is often
required to confirm such motility disturbances.
Once a cause of dysphagia has been established, management will depend
on the cause. Strictures secondary to gastroesophageal reflux disease are man-
aged with periodic esophageal dilations and long-term proton pump inhibitors
(e.g., omeprazole). Esophageal strictures can be dilated following endoscopy.
Esophageal carcinoma requires either surgery, radiation or palliative insertion
of prosthesis. Esophageal motility disturbances can sometimes be managed
medically with nitroglycerin or calcium channel blocking agents. Achalasia and

esophageal spasm sometimes require surgical myotomy or pneumatic dilation.
5. DYSPEPSIA / C. Dubé
5.1 Description
Dyspepsia refers to chronic or recurrent pain or discomfort centered in the
upper abdomen. Individuals might refer to this symptom as “indigestion.”
Bloating, early satiety, nausea, and vomiting are other symptoms that may
also be reported in association with dyspepsia. Dyspepsia can be intermittent
or continuous, and, importantly, may or may not be related to meals.
5.2 Etiology
The major organic diseases causing dyspepsia are gastroduodenal ulcer,
atypical gastroesophageal reflux, and gastric cancer. Up to 60 % of patients
with dyspepsia have no definite explanation and are classified as having func-
tional (idiopathic) dyspepsia, also referred to as nonulcer dyspepsia. The
pathophysiology of functional dyspepsia is unclear. Factors such as gastric
motor dysfunction, visceral hypersensitivity, psychosocial factors and
Helicobacter pylori infection might play a role in its pathophysiology.
5.3 History and Physical Examination

It is impossible to differentiate between organic and functional dyspepsia on
the basis of the patient’s description of the symptom alone. Similarly, the pres-
ence of epigastric pain on physical examination is not discriminating. It is
therefore important to look for clues to an organic etiology of the dyspepsia,
so-called alarm features, such as gastrointestinal bleeding, symptoms of
anemia, a history of weight loss, or the presence of an epigastric mass or
hepatomegaly on physical examination. Peritoneal signs or a succession
splash would be suggestive of free ulcer perforation and gastric outlet
obstruction respectively.
Careful history will also help differentiate between dyspepsia and gastro-
esophageal reflux disease (GERD), irritable bowel syndrome (IBS), and biliary
colic. Up to a third of GERD sufferers do experience epigastric pain or dis-
comfort that is centered in the epigastrium. However, in such cases, symptoms
of heartburn and regurgitation, often recumbency-aggravated, will usually be
associated. Bloating and epigastric pain or discomfort may also occur in IBS.
However, this is generally distinguished from dyspepsia by its association
with altered bowel habits, as well as the relief of the pain with defecation.
There should be no confusion between the episodic nature and severity of pain
due to biliary colic or pancreatic disease and the more predicable and regular
occurrence of dyspepsia. Indeed, dyspeptic symptoms are equally common in

those who have and in those who do not have gallstones.

In younger patients with no alarm features who have not been investigated
previously, it is recommended that a noninvasive H. pylori test (e.g., serology
or urea breath test) is undertaken to determine if the patient is infected. If there
is documented H. pylori infection, then an empiric trial of anti-H. pylori therapy
is recommended. The rationale is that ulcer disease will heal and the ulcer
diathesis will be abolished. If symptoms fail to respond or rapidly recur or
alarm features develop, then prompt upper endoscopy is indicated. In younger
patients with no alarm features who are H. pylori negative, and who have
persistent symptoms, one option is to opt for a therapeutic trial of antisecretory
therapy (e.g., H2-blocker or proton pump inhibitor) or of a prokinetic agent.
If symptoms persist or rapidly recur on stopping treatment, then endoscopy
is recommended. It is worth noting that endoscopy is the test of choice to
exclude gastroduodenal ulceration, reflux esophagitis, and upper gastrointestinal
tract malignancy. Although upper gastrointestinal radiographs have inferior
diagnostic accuracy to upper endoscopy, they are more accessible and cheaper.
Another option is to refer all dyspepsia sufferers to prompt endoscopy, since
investigations for dyspepsia in the setting of low clinical suspicion for organic
disease have the added advantage of providing reassurance to the patient, a
strategy with proven therapeutic efficacy.
Referral for early upper endoscopy is always indicated in older patients
presenting with new-onset dyspepsia. This is because the incidence of gastric
cancer increases with advancing age; a threshold of 45 years is recommended.
As mentioned above, patients with alarm symptoms (e.g., weight loss, recur-
rent vomiting, dysphagia, evidence of bleeding, or anemia) and patients
whose symptoms have failed to respond to empiric therapeutic approaches
should undergo endoscopy.
6. NAUSEA AND VOMITING / M.C. Champion
6.1 Synonyms
Barf, upchuck, bring up.
6.2 Description
Nausea is a psychic as well as physical experience and defies precise
definition. Vomiting is evacuation of the stomach contents through the mouth.
Nausea normally precedes vomiting. There can be associated tachycardia,
hypersalivation, waterbrash and excessive perspiration.
6.3 Mechanism (Figure 1)

A variety of stimuli may produce nausea (labyrinthine stimulation, pain,
unpleasant memories). The neural pathways mediating nausea are not known,
but evidence suggests that they are the same pathways that mediate vomiting.
During nausea, gastric tone and peristalsis are reduced. The tone of the duode-
num and proximal jejunum tends to be increased, with frequent reflux of
duodenal contents into the stomach.
Vomiting occurs as the gastric contents are forcefully brought up to and out
of the mouth. This occurs by forceful sustained contraction of the abdominal
muscles at a time when the cardia of the stomach is raised and open and the
pylorus is contracted. Elevation of the cardia eliminates the intra-abdominal
portion of the esophagus and relaxes the lower esophageal sphincter. This
allows the stomach contents to enter the esophagus. The act of vomiting is
completed with rapid upward displacement of the diaphragm and reversal of
thoracic pressure from negative to positive. The glottis closes, the soft palate
rises, the mouth opens and the stomach contents are expelled. The control of
vomiting consists of two anatomically and functionally separate units, a vom-
iting center and a chemoreceptor trigger zone. The vomiting center is in the
reticular formation of the medulla and is excited directly by visceral afferent
impulses (sympathetic and vagal) arising from the gastrointestinal tract and
other peripheral trigger areas. These trigger areas are found in the pharynx,
cardiac vessels, peritoneum, bile ducts, cortex and stomach. The chemorecep-
tor trigger zone is on the floor of the fourth ventricle, on the blood side of the
blood–brain barrier. The chemoreceptor trigger zone is unable to cause vomit-
ing without an intact vomiting center.
6.4 History and Physical

Patients may complain of nausea and hypersalivation. With gastrointestinal
causes of the nausea (and vomiting) there may be associated symptoms of
heartburn or epigastric pain. Prior to vomiting, patients may retch (spasmod-
ic, abortive respiratory movements with the glottis closed).
History-taking should probe for precipitating factors, other symptoms that
suggest the underlying cause, drug use and dietary habits. The history should
also explore psychological trauma or disturbances of body image suggestive
of anorexia nervosa.
Physical examination is often normal. An abdominal mass may point to
an underlying cause (e.g., gastric carcinoma). Prolonged vomiting may
cause dehydration.
6.5 Differential Diagnosis

Prolonged nausea, by itself, rarely has an organic origin. There are many causes
FIGURE 1. The vomiting center and chemoreceptor trigger zone control vomiting. Peripheral
trigger areas send visceral afferent impulses, which excite the vomiting center into action.
of nausea and vomiting, including intracerebral problems (e.g., hydrocephalus,

brain tumor), stimulation of the peripheral trigger areas (e.g., severe chest
pain, pain from kidney stones), systemic disease (malignancy), medications
and pregnancy. Upper gastrointestinal diseases (esophagitis, peptic ulcer dis-
ease, gastric carcinoma) are common. Early morning nausea and vomiting
suggest pregnancy, gastroesophageal reflux disease, alcohol withdrawal, a
metabolic cause (e.g., uremia) or a psychogenic origin.

In approaching a patient with nausea and vomiting, one should look for and
correct any underlying causes. Prolonged vomiting may cause dehydration
and the patient may need to be rehydrated intravenously. Medications should
be discontinued.
There are many drugs that have anti-emetic actions. Antihistamines act on
the vestibular apparatus as well as on the chemoreceptor trigger zone.
Phenothiazines also exert their action on the chemoreceptor trigger zone.

Metoclopramide and domperidone are both anti-emetics and gastric proki-
netics (which stimulate the stomach to empty). Domperidone exerts its
action on the chemoreceptor trigger zone, whereas metoclopramide also
crosses the blood-brain barrier and affects the vomiting center. Cisapride, a
newer gastric prokinetic, has no effect on the chemoreceptor trigger zone or
vomiting center. Like the other prokinetic agents, it may improve nausea
and vomiting if they are due to gastric stasis or gastroparesis.
7. ANOREXIA / M.C. Champion
7.1 Description
Anorexia is the lack (or loss) of appetite. Anorexia is a common and impor-
tant, but nonspecific, symptom. It can be a presenting feature in patients with
organic or psychological disease. Anorexia and weight loss may be the early
signs of malignancy.
7.2 Mechanism
The hypothalamus plays a major role in regulating the intake of food. At one
time it was generally held that a “satiety center” and a “feeding center” in the
hypothalamus exerted the fundamental control over food intake. Stimulation
of the satiety center was believed to inhibit the feeding center and gastric
hunger contractions. The feeding center was considered to be an integrative
station that coordinates complex reflexes associated with food intake. How-
ever, it is now believed that control of appetite is best considered as multiple
neuropharmacologic interactions in the hypothalamus rather than the effect of
a distinct satiety center and feeding center.
7.3 History and Physical

The history should detect other symptoms that may suggest underlying
organic or psychological disease. A calorie count is also helpful to assess the
actual intake of food. The amount and duration of weight loss should also
be documented.
Physical examination may be normal except for evidence of weight loss.
It may point to the underlying organic problem, such as cardiac failure
or malignancy.

Many (and perhaps most) illnesses feature a loss of appetite. These range from
gastrointestinal disease to malignancy, chronic renal failure, congestive heart
failure and many psychiatric diseases, such as depression and anorexia nervosa.
7.5 Approach to Investigation and Management

Investigation should exclude organic disease. The approach depends upon the
patient’s symptoms and signs. If no physical ailment is discovered, careful
screening may be necessary to exclude psychiatric disease.
8. GAS AND BLOATING / W.G. Thompson
8.1 Synonyms and Related Terms

Burbulence, flatulence, burp, belch, borborygmi, gaseous distention, wind,
flatus, fart.
Gas and bloating embrace three unrelated phenomena. Farting is a physio-
logic phenomenon due to the production of gas by colon bacteria. Excessive
belching or burping is associated with aerophagia (air swallowing). This is
also partly physiological, but it may become exaggerated through habit. The
mechanism of bloating is obscure. These phenomena are unrelated, yet they
often occur together.
8.2 Farting, Gas, Wind, Flatus
8.2.1 MECHANISM
Farting is a physiologic excretory process. Normally, the gut contains
100 to 200 mL of gas. An average person on a normal diet emits about 1 L
per day. We pass 50 to 500 mL a mean of 13.6 times per day, although there
is great variation from person to person and from time to time. Those prone
to produce greater amounts of gas or who are unduly sensitive may suffer
socially. Most emitted gas originates in the colon. Some carbohydrates such
as cellulose, glycoproteins and other ingested materials, not assimilated in the
small intestine, arrive intact in the colon where resident bacteria digest them
to produce hydrogen, carbon dioxide, methane and trace gases.
Intestinal floras differ from person to person. Some bacteria produce
hydrogen, while others consume it. In one person out of three, an organism
called Methanobrevibacter smithii converts hydrogen to methane. The
presence of this organism and the methane-producing trait are a result
of early environment. Spouses do not share the trait with one another.
Another product of fermentation, carbon dioxide, is also released when
hydrochloric acid reacts with bicarbonate in the intestines. However, this
gas is quickly absorbed. Hydrogen, carbon dioxide, methane and swal-
lowed nitrogen comprise 99% of colon gas. The remaining 1% consists of
trace gases that compensate for their small quantities by their strong odors.
Smelly gases include hydrogen sulfide ammonia, skatole, indole and
volatile fatty acids.
Borborygmi is the name given to the noises generated as air and fluid
gurgle through the gut. Bloating is not due to excessive gas.
8.3 Aerophagia
8.3.1 MECHANISM
During inspiration, the normally negative intraesophageal pressure draws in
ambient air. Forced inspiration against a closed glottis (intentionally closed
windpipe) draws in even more air. The air may be forced out again as intra-
esophageal pressure increases with expiration. Adolescents love to shock their
elders with voluntary belching. As a practical application, those who have lost
their larynx because of cancer put this learnable skill to use in generating
esophageal speech. More commonly, aerophagia is an unwanted but learned
habit in those who repeatedly belch in response to other gut symptoms.
Some air is ingested with each swallow, perhaps more with food. Nervous
patients undergoing abdominal x-rays accumulate more intestinal gas than
those who are relaxed. Other mechanisms of aerophagia include thumb suck-
ing, gum chewing, drinking carbonated drinks, rapid eating and wearing poor
dentures. Stomach gas has the same composition as the atmosphere.
In achalasia, where the lower esophageal sphincter cannot relax, the stom-
ach is gasless. In bowel obstruction or a gastrocolic fistula colon gases reach
the stomach. Sometimes gastric stasis permits bacteria to grow and produce
hydrogen in the stomach. Normally, gastric gas is swallowed air.
8.3.2 CLINICAL MANIFESTATIONS OF AEROPHAGIA

Belching is to bring forth wind noisily from the stomach. The word burp means
to “cause to belch,” as one would burp a baby, but colloquially, the terms are used
interchangeably. A belch after a large meal is a physiologic venting of air from
the stomach. A meal stretching the muscle of the stomach, which can stretch to
accommodate food, causes distress with little increase in intragastric pressure.
A satisfying belch eases the discomfort. Some individuals seem unduly sensitive
to intragastric pressure. People with gastroenteritis, heartburn or ulcers swallow
more frequently. If release of gas transiently relieves the distended feeling, a
cycle of air swallowing and belching may be established. The swallow-belch
cycle may continue long after the original discomfort is forgotten.
Of course, venting gas is important, as those unable to do so will attest.
When the lower esophageal sphincter is reinforced by antireflux surgery,
belching may be impossible. Bedridden patients such as those recovering
from surgery may trap air in the stomach. In the supine position gastric
contents seal the gastroesophageal junction so that air cannot escape until the
subject assumes the prone position.
While a patient may insist that his or her stomach is producing prodigious
amounts of gas, in reality air is drawn into the esophagus and released. A little
may even reach the stomach. Some can belch on command, and the inspiration
against a closed glottis is demonstrable. Most sufferers are relieved
to have their habit pointed out, but some are incredulous. Quitting the habit
is often difficult. Repeated and intractable belching is termed eructio nervosa.
8.4 Functional Abdominal Bloating
8.4.1 MECHANISM
Those complaining of bloating and distention are often convinced that it is due
to exess intestinal gas. Although the sensation may induce aerophagia, it sel-
dom results from it. Farting may temporarily relieve bloating, but intestinal gas
production does not cause it. Research has demonstrated that gas volume in
bloaters is not abnormal. Despite visible distention, x-rays and computerized
tomography (CT) show no large collections of intestinal gas. The distention
disappears with sleep and general anesthesia.
Gut hypersensitivity may explain the sensation of abdominal bloating. The
hypersensitive gut feels full at lower than normal filling, and abdominal mus-
cles relax to accommodate the perceived distention. The stomach is and feels
distended with normal amounts of air.
Abdominal girth of female irritable bowel syndrome (IBS) patients
complaining of distention may increase 3–4 cm over an eight-hour day. CT
has demonstrated the change in profile despite unchanged gas content or dis-
tribution. There were no corresponding changes in control subjects. Lumbar
lordosis (arching of the spine) is sometimes increased. When women deliber-
ately protrude their abdomens, the configuration is different from when they
are bloated, so a conscious mechanism poorly explains increased abdominal
girth. Perhaps abdominal muscles are weakened. The reality of the phenomenon
is indisputable; the mechanism remains a mystery.
8.4.2 CLINICAL FEATURES

Bloating occurs in 30% of adults and is frequent in 10%. Amongst those
with the irritable bowel syndrome and dyspepsia the figures are much high-
er. It is often the most troublesome feature of these conditions. Typically,
the abdomen is flat upon awakening, but distends progressively during the
day, only for the distention to disappear with sleep. Women complain of the
need to let out their clothing and sometimes volunteer “It’s as if I’m six
months pregnant.” Many report that bloating occurs quickly, in some cases
within a minute. It is often aggravated by eating and relieved by lying
down. Menstrual periods and stress affect a few cases. Usually, it is most
obvious in the lower abdomen, but many report it near the umbilicus or all
over the belly.
8.4.3 DIFFERENTIAL DIAGNOSIS

Observable bloating has been called hysterical nongaseous bloating, pseudo-
tumor or pseudocyesis (false pregnancy). If distention is present at the time of
the examination (more likely late in the day) and absent on other occasions,
the phenomenon is likely functional. There is no abdominal tympany to
suggest gaseous intestines, and sometimes the distended abdomen can be mis-
taken for ascites or a tumor.
Bloating is often associated with dyspepsia or IBS. On its own, it is not a
symptom of organic disease and should prompt no investigation. In intestinal
obstruction or postoperative ileus (paralyzed intestines), gas accumulates and
distends the gut to cause discomfort and pain. In such a case, there are other
symptoms and signs with which to make a diagnosis.
9. CONSTIPATION / C. Dubé and W.G. Thompson
9.1 Synonyms
Costiveness, obstipation.
9.2 Description
Constipation defies accurate definition. What is “normal” frequency?
Ninety- five percent or more of the population have between three move-
ments per day and three movements per week. Some people consider that
fewer than three movements a week without discomfort or dissatisfaction
is normal. The effort needed to pass the stool and the consistency of the
stool are probably of greater importance. Most would agree that hard
bowel movements that are difficult to pass constitute constipation even if
they occur as often as daily. One definition of constipation is the need to
strain at stool on more than 25% of occasions. Thus constipation is
defined as persistent symptoms of difficult evacuation, including strain-
ing, stools that are excessively hard, unproductive urges, infrequency, and
a feeling of incomplete evacuation.
9.3 Mechanism
Constipation may be due to primary colonic conditions, such as obstructing
lesions of the colon, irritable bowel syndrome and idiopathic slow-transit
constipation. It may also be caused by systemic afflictions, either endocrine
(diabetes mellitus, hypothyroidism), metabolic (hypo- or hypercalcemia),
TABLE 1. Some causes of chronic constipation
Primary diseases of the colon Pharmacologic

Stricture Opiates
Cancer Antidepressants
Anal fissure Antispasmodics
Proctitis Calcium channel blockers
Irritable bowel syndrome Iron
Idiopathic slow-transit constipation Laxative abuse
Pelvic floor dyssynergia Neurologic and muscular disorders

Parkinson’s disease
Metabolic disturbances Spinal cord lesion
Hypercalcemia Multiple sclerosis
Hypocalcemia Autonomic neuropathy
Hypothyroidism Hirschsprung’s disease
Diabetes mellitus Systemic sclerosis
Pregnancy Myotonic dystrophy
neurologic (multiple sclerosis, Parkinson’s disease), muscular (systemic scle-

rosis, myotonic dystrophy), or medications (opiates, anticholinergic agents,
antihypertensives). The most common kind of constipation is that associated
with the irritable bowel syndrome (Table 1).
Proper defecation requires normal transit through the proximal colon, an intact
gastrocolonic response to a meal, and normal mechanisms of defecation, involv-
ing: (1) the defecation reflex (i.e., the presence of stool in the rectum initiating
the evacuating response of the internal sphincter); (2) the coordinated relaxation
of the puborectalis and external anal sphincter muscles; (3) adequate functional
anatomy of the rectal outlet together with (4) increased intra-abdominal pressure;
and (5) inhibition of colonic segmenting activity. Any failure at any level of col-
orectal function may therefore lead to constipation.
9.4 Important Points on History and Physical

A detailed dietary history with respect to the daily intake of fibre and liquids
as well as eating patterns is important: the majority of constipated patients do
not eat breakfast, which is an important trigger of the gastro-colonic response.
Physical impairments and bedridden states will also contribute to constipa-
tion. The list of medications should be reviewed and a history of prolonged
intake of cathartics, often in the form of herbal remedies or teas, should be
sought. Symptoms suggestive of IBS, such as bloating, abdominal pain, and
alternation of diarrhea with constipation should be enquired about. History

also includes symptoms related to pelvic descent, such as stress incontinence.
A history of weight loss, of a recent onset of constipation, of the presence of
blood around the stools, as well as the presence of risk factors for colorectal
cancer, should raise the possibility of an obstructing carcinoma.
On physical examination, one should note the presence of abdominal
distension or of palpable stools, either in the left lower quadrant or in the
more proximal colon. Rectal examination is useful to identify fissures or
hemorrhoids which may either cause or be caused by constipation. A lax or
asymmetric anal opening may suggest a neurologic disorder with impaired
sphincter function, and the presence of stools in the rectum may suggest an
impaired defecation reflex.
9.5 Approach to Diagnosis

Sigmoidoscopic examination using either the rigid or flexible instrument is nec-
essary to rule out local diseases such as fissures, fistulas or distal proctitis. Many
cancers are within the range of the sigmoidoscope. One might also detect
melanosis coli, a pigment in the rectal mucosa that indicates chronic laxative use.
If the constipated patient is over 40, has blood or pus in the stool, or has had
significant weight loss, a colonoscopy is indicated to rule out cancer, polyps
or Crohn’s disease of the colon. Barium enema may be useful to assess for
megarectum or megacolon, but distal rectal lesions may be missed, so sig-
moidoscopic examination should not be foregone.
A gut transit study may be revealing. Twenty radiopaque markers are
ingested and daily plain abdominal x-rays are taken. If 80% of the markers
have disappeared in five days, the transit time is said to be normal. In cases
of longer transit, the position of the markers may help distinguish colonic
inertia from anorectal disorder. More sophisticated studies, such as anorectal
manometry and defecography, are then required.
9.6 Approach to Management

Management of constipation includes education as to the great variability of
bowel habits among the general population, reassurance as to the benign
nature of the condition once appropriate investigations have been carried out,
dietary changes, and judicious use of laxatives. Dietary changes include the
intake of at least three meals a day, the first meal of the day being taken upon
arousal. Adequate amounts of liquids, such as 6 to 8 cups per day, should be
ingested, and a high fibre diet, either with the intake of roughage and cereals
or with the addition of bulk-forming agents, should be achieved. The recom-
mended amount of dietary fiber is 20 to 35 g/day.
Chronic severe constipation may require the daily use of osmotic agents
such as lactulose or sorbitol, of polyethylene glycol solution, or of pharmaco-
logic agents, such as tegaserod. The long-term use of stimulant laxatives such
as bisacodyl or senna should be avoided.
10. DIARRHEA / W.G. Thompson
10.1 Synonyms
Lax bowels, the flux.
10.2 Description
Diarrhea is best described as too frequent passage of too loose (unformed)
stools. Diarrhea is frequently accompanied by urgency, and occasionally
incontinence. When considering a patient with diarrhea the following
must be considered: frequency (> 3 movements/day), consistency (loose/
watery), urgency, volume (> 200 g/day) and whether the condition is
continuous. Persistent, frequent, loose, urgent, large-volume stools are
most likely to have a pathology. Lesser and intermittent symptoms are
more likely to be functional.
10.3 Mechanism
Diarrhea is due to one or more of four mechanisms: osmotic attraction of
excess water into the lumen of the gut, secretion of excess fluid into the gut
(or decreased absorption), exudation of fluid from the inflamed surface of the
gut, and rapid gastrointestinal transit.
Osmotic diarrhea results if the osmotic pressure of intestinal contents
is higher than that of the serum. This may result from malabsorption of fat
(e.g., in celiac disease) or of lactose (e.g., in intestinal lactase deficiency).
Certain laxatives, such as lactulose and magnesium hydroxide, exert their
cathartic effect largely through osmosis. Certain artificial sweeteners, such as
sorbitol and mannitol, have a similar effect. Characteristically, osmotic diar-
rhea ceases when the patient fasts.
Secretory diarrhea occurs when there is a net secretion of water into the lumen.
This may occur with bacterial toxins, such as those produced by E. coli or Vib-
rio cholerae, or with hormones, such as vasoactive intestinal polypeptide (VIP),
which is produced by rare islet cell tumors (pancreatic cholera). These provoke
adenylate cyclase activity in the enterocyte (intestinal epithelial cell), increase
cyclic AMP and turn on intestinal secretion. A similar effect may occur as a result
of excess bile salts in the colon (choleretic enteropathy) and from the cathartic
effect of hydroxylated fatty acids resulting from the bacterial action on
malabsorbed fat. Such a diarrhea does not diminish with fasting. Osmotic and
secretory diarrhea result from abnormalities in the small intestine such that the
flow of water through the ileocecal area overcomes the absorptive capacity of
the colon.
Exudative diarrhea results from direct damage to the small or large intesti-
nal mucosa. This interferes with the absorption of sodium salts and water and
is complicated by exudation of serum proteins, blood and pus. Infectious or
inflammatory disorders of the gut cause this kind of diarrhea.
Acceleration of intestinal transit may result in diarrhea (e.g., as a result of
hyperthyroidism). The rapid flow-through impairs the ability of the gut to
absorb water, resulting in diarrhea.
In most instances of diarrhea two or more of these four mechanisms are at
work, so these pathogenetic concepts are seldom of great help in diagnosis.
10.4 Important Historical Points and Physical Examination Features

It is important to establish the frequency of defecation, the duration of the
diarrhea, the nature of the stool and its volume. If diarrhea has been present
for less than two weeks, it is most likely a result of an infection or toxin. A
history of many previous attacks, on the other hand, may indicate a recurrence
of inflammatory bowel disease. The frequency of the stool gives some idea of
severity; one should establish whether incontinence is also present. To elicit
the latter history may require direct questions. Stool from malabsorption is
often foul-smelling and contains oil droplets. A history of nutrient deficiency,
anemia or weight loss also suggests malabsorption. Watery diarrhea, particu-
larly when large in volume, supports a diagnosis of small bowel disease.
However, a large villous adenoma of the distal colon may produce a watery
diarrhea. The presence of blood or pus in the stool suggests an exudative diar-
rhea, a type of diarrhea that is often relatively small in volume and indicative
of colitis. Loose bowel movements interspersed with normal or even consti-
pated ones are evidence of the irritable bowel syndrome.
There are many causes of diarrhea, some of which are summarized in
Table 2. The presence of profound weight loss and malnutrition in a young
person points to a malabsorption syndrome due to small bowel or pancreatic
disease or to inflammatory bowel disease. Metabolic conditions such as
hyperthyroidism or the overuse of (magnesium-containing) antacids or laxa-
tives might also be responsible for chronic diarrhea.
Travel to tropical countries can be marred by an attack of so-called traveler’s
diarrhea. The most common cause is toxigenic E. coli (it is known as toxigenic
because a toxin is produced). However, a large variety of intestinal infestations
can occur with travel. Pseudomembranous colitis may occur within weeks of
the use of antibiotics. Campylobacter or cryptococcosis may be acquired from
TABLE 2. Anatomic approach to the causes of chronic diarrhea
Gastric
Dumping syndrome
Small intestine
Celiac disease
Lymphoma
Whipple’s disease
Parasitic infection (Giardia lamblia)
Abnormal intestinal tract motility with bacterial overgrowth (scleroderma, amyloidosis,
diabetes, hyperthyroidism)
Large bowel
Villous adenoma (adenocarcinoma)
Inflammatory bowel disease (ulcerative colitis, Crohn’s disease)
Irritable bowel (diarrhea phase)
Functional diarrhea
AIDS-related infections
Pancreatic
Chronic pancreatitis
Islet cell tumors
Gastrin secretions
VIP secretions
Drugs
Antacids
Antibiotics
Alcohol
Antimetabolites
Laxatives
Digitalis
Colchicine
Sorbitol, fructose
Many others
Metabolic
Hyperthyroidism
Hypoparathyroidism
Addison’s disease
Diabetes
Carcinoid syndrome
pets. Contaminated water may result in giardiasis, amebiasis or cryptococcosis.

Chronic use of alcohol may damage the small intestinal mucosa. Diabetics
frequently have diarrhea because of autonomic neuropathy, perhaps with bacte-
rial overgrowth.
Finally, it is essential to establish if the patient is homosexual. Almost any
of the usual gastrointestinal pathogens can be spread by homosexual activity,
including lymphogranuloma venereum and gonococcus. In addition to the
“gay bowel syndrome,” homosexuals are liable to the gastrointestinal compli-
cations of AIDS.
10.5 Differential Diagnosis and Management

The recent onset of acute diarrhea requires careful examination of the stool for
pus cells and culture for bacterial pathogens, or a study for ova and parasites
in the case of suspected protozoa. Viral studies are important in infants, and
special studies are required in AIDS.
The differential diagnosis of chronic diarrhea is very complex. A careful
history is often the most important diagnostic tool. Patients examined for the
first time deserve at least a sigmoidoscopy to rule out local colon disease. If a
small intestinal diarrhea is suspected, a three-day collection of stool to deter-
mine daily weight and fat content is necessary. If there is steatorrhea, or if
stool weight exceeds 500 g per day, there is likely to be small intestinal or
pancreatic disease. Smaller volumes, particularly if accompanied by blood,
point to inflammation of the colon.
11. MALNUTRITION / D.G. Patel
11.1 Description
Nutrition may be defined as the process by which an organism utilizes food.
This complex process involves ingestion, digestion, absorption, transport,
utilization and excretion. Any alteration in one or many of these factors can
produce malnutrition. Globally, primary malnutrition due to lack of food is the
most common cause of malnutrition. Malnutrition in the Western world is
mainly due to inadequate intake of nutrients, malabsorption and/or the hyper-
catabolism accompanying a critical illness. Protein-energy undernutrition is
increasingly recognized in eating disorders such as anorexia nervosa.
11.2 Mechanism
The malnutrition associated with gastrointestinal disorders is usually
multifactorial and varies with the nature and activity of the disease.
1. Lack of food intake due to anorexia or food-related symptoms such as

dysphagia, pain or vomiting.
2. Maldigestion due to pancreatic disease. Deficiency of bile salts due to
cholestatic hepatobiliary disease or to ileal disease leads to maldigestion
of triglyceride and lipid-soluble vitamins. Steatorrhea (fat malabsorption)
produces negative caloric balance and deficiency of fat-soluble vitamins.
3. Malabsorption due to mucosal disease of the small intestine or loss of
surface area due to intestinal bypass, fistula or resection.
4. Excessive loss of nutrients, as in protein-losing enteropathy and loss of
zinc in diarrheal illness.
5. Therapeutic agents that may selectively affect nutrient utilization – e.g.,
cholestyramine use for bile acid–induced diarrhea can worsen steatorrhea.
6. Alcoholism – an extremely common cause of malnutrition in the Western
world. Social and economic status, behavior problems, isolation and
depression cause reduced intake of nutrients. Alcoholics rarely consume
a well-balanced diet and depend very heavily on “empty” calories from
alcohol. Protein and vitamin deficiencies, particularly of the B-complex
group, are extremely common. Alcohol is a toxic agent that even in the
presence of adequate nutritional intake can produce damage to the pan-
creas, liver and small bowel mucosa, aggravating malnutrition.
11.3 Signs of Malnutrition
1. Weight loss in the absence of edema is a good indicator of energy deficiency.

2. Muscle wasting, particularly in the temporal area and dorsum of the hand
between thumb and index finger, suggests protein-calorie deficiency.
3. Dry, scaly skin with pigmentation results from vitamin and trace metal
deficiency.
4. Angular mouth fissure (cheilosis) is due to riboflavin deficiency.
5. Glossitis and depapillation of the tongue are due to B12, folate or iron
deficiency.
6. Hepatomegaly may be due to fatty liver, a common finding in protein
malnutrition or alcoholism.
7. Peripheral neuropathy (decreased position sense), decreased vibration
sense or ataxia may result from B12 deficiency.
8. Weakness and paresthesia of the legs are signs of nutritional polyneuro-
pathy, especially in alcoholics (due to thiamine or pyridoxine deficiency).
9. Anemia due to iron, folate or B12 deficiency or chronic disorders.
10. Peripheral edema.
11. Hypoalbuminemia.
12. ACUTE ABDOMEN / J.M. Watters
12.1 Description
The term acute abdomen is best used to describe abdominal pain and related
symptoms and signs that are sufficiently severe as to suggest a serious intra-
abdominal condition. Pain has usually been present for 72 hours or less and
sometimes for only a few hours. Since some patients with an acute abdomen
require resuscitation and early surgical treatment, it is important to assess the
patient and establish a plan of management as soon as possible. The initial
goal is not necessarily to make a definitive diagnosis, but rather to identify
those patients who require prompt surgical intervention.
12.2 Mechanism
Acute abdominal pain may be referred to the abdominal wall from intra-
abdominal organs (visceral pain) or may involve direct stimulation of the
somatic nerves in the abdominal wall (somatic pain). The nerve supply to the
viscera is bilateral, and visceral pain is not usually lateralized. Foregut pain is
typically epigastric in location, midgut pain is central, and hindgut pain is felt
in the lower abdomen. Organs that are bilateral give rise to pain that is
predominantly felt on one or the other side of the body. Visceral pain arises
from tension in the bowel wall (e.g., distension or vigorous contraction),
mesenteric traction, or irritation of the mucosa or serosa of the bowel
(e.g., chemical irritation, bacterial contamination, ischemia).
Somatic pain is more precise in location than visceral pain and corresponds
more directly to the anatomic site of the underlying pathology. Occasionally,
pain is referred to the abdomen from extra-abdominal sites (e.g., lower lobe
pneumonia). Unusually, acute abdominal pain is a feature of systemic disease
(e.g., diabetic ketoacidosis). Somatic pain occurs with stimulation of pain
receptors in the peritoneum and abdominal wall.
12.3 History
The initial location and character of acute abdominal pain and their subse-
quent evolution often give useful clues to the site and nature of the under-
lying pathology. A history of pain with movement (e.g., riding in a car or
walking) suggests the presence of peritonitis if it is not otherwise obvious.
Steady, severe pain is more ominous than colicky pain. Severe pain of
sudden onset suggests a catastrophic event (e.g., perforation of an ulcer,
intestinal ischemia, or rupture of aortic aneurysm). Colicky pain corre-
sponds to peristaltic waves and eases or disappears between waves. Exam-
ples are the intermittent, mid-abdominal pain of uncomplicated small
bowel obstruction and the intermittent flank pain radiating anteriorly to
the groin accompanying ureteric obstruction. However, when the viability

of obstructed small bowel is comprised, for example, the now-ischemic
segment of bowel causes unremitting pain that is localized to the area of the
involved loop. Biliary “colic” is a misnomer in that the pain is typically
steady. It is usually epigastric or upper abdominal and relatively diffuse,
becoming more localized in the right upper quadrant if the process evolves
into acute cholecystitis.
Radiation of pain may provide important clues to diagnosis. Irritation of
the diaphragm, from blood in the peritoneal cavity, for example, may cause
shoulder tip pain. Biliary tract pain may radiate to the right scapular region.
Pain arising from retroperitoneal structures may be perceived in the back
(e.g., pancreatitis, leaking abdominal aortic aneurysm).
12.4 Associated Symptoms

Anorexia, nausea and vomiting are more common in diseases of the gastroin-
testinal tract and not specific in terms of diagnosis. Abdominal distention and
obstipation accompanying acute abdominal pain suggest intestinal obstruc-
tion. In a patient with colonic obstruction and/or perforation, a recent change
in bowel habit or blood in the stool (prior to the onset of pain) suggests
the possibility of a colon cancer. Bloody diarrhea may arise from severely
inflamed, ulcerated or infarcted bowel. In women an accurate menstrual
history aids the diagnosis of ovarian disease, ectopic pregnancy and pelvic
inflammatory disease. Urinary symptoms may suggest a genito-urinary
diagnosis (e.g., pyelonephritis, renal stones).
12.5 Physical Examination

Examination of the abdomen is normally carried out with the patient supine.
Analgesia may impair the sensitivity of physical examination when signs are
subtle, but should be given promptly once assessment has been completed or
when it will be unavoidably delayed. When the presenting pain is severe,
alleviating it may well permit a more useful history and subtle examination
to be obtained.
Inspection of the abdomen should note any distention or masses. The
patient with peritonitis typically lies immobile, since any movement increases
peritoneal irritation and pain. With ureteral colic, the patient may appear rest-
less, seeking a more comfortable position.
Auscultation may reveal a range of bowel sounds, from the silent abdomen
of peritonitis to the hyperactive sounds of bowel obstruction. Bruits suggest
vascular disease, but an epigastric bruit may also be found normally.
Gentleness is the key to palpation. Palpation detects and localizes tender-
ness, muscle guarding, rigidity and masses. Guarding refers to the involuntary
contraction of initially relaxed muscles of the abdominal wall in response to

the pain stimulated or exacerbated by palpation. Guarding may be localized
(e.g., uncomplicated appendicitis) or generalized throughout the abdomen
(e.g., perforated diverticulitis with diffuse contamination of the peritoneal
cavity). In some instances (e.g., perforated duodenal ulcer), the muscles are in
a state of continuous contraction and are rigid or “board-like” even without
palpation. In subtle situations, peritonitis is suggested by the triggering of pain
in the area of suspected pathology (e.g., appendicitis) through palpation else-
where on the abdominal wall, by having the patient cough or by gently shak-
ing the pelvis. Gentle percussion is also a very useful way to assess peritoneal
irrigation, as well as to assess the nature of abdominal distention. Testing for
“rebound” tenderness by deeply palpating the area of concern and then sud-
denly releasing the abdominal wall is very distressing to the patient with
peritonitis, may be misleading in the patient without peritonitis, and does
not contribute to diagnosis.
Rectal and pelvic examination should be carried out and recorded by at
least one examiner. The sites for inguinal and femoral hernias should be
specifically examined. Femoral pulses should be palpated. A careful physical
examination will identify pertinent extra-abdominal findings (e.g., jaundice,
lymphadenopathy), systemic effects of an acute abdominal condition (e.g.,
hypotension, tachycardia, tachypnea), and significant coexisting conditions.

Intra-abdominal conditions requiring surgery (open or laparoscopic) are the
most common causes of an acute abdomen. Some conditions require imme-
diate surgery (e.g., ruptured abdominal aneurysm). They must always be
included in the differential diagnosis, therefore, and confirmed or excluded
promptly. In other instances, the specific diagnosis and the need for surgery
may take some time to establish. The likelihood of specific diagnoses varies
to an extent with the age of the patient. Clinical presentations are more like-
ly to be atypical in the elderly and in patients with coexisting conditions
(such as diabetes or stroke). Particular care must be taken to not overlook an
important intra-abdominal process in such patients.
One must always consider in the differential diagnosis: (1) intra-abdominal con-
ditions for which surgery is not indicated (e.g., acute pancreatitis, primary bacte-
rial peritonitis); and (2) extra-abdominal (e.g., pneumonia) or systemic conditions
(e.g., diabetic ketoacidosis) that can be accompanied by acute abdominal pain.
12.7 Investigations
In many instances, a careful history and physical examination provide the
clinical diagnosis. Complete blood count (CBC) and urinalysis are routine.
Serum amylase or lipases, electrolytes, creatinine and glucose are frequently

obtained. Other blood work is obtained as indicated. Chest and plain abdomi-
nal x-rays are obtained routinely unless the diagnosis is clear (e.g., appendici-
tis). Free intraperitoneal air, suggesting a perforated viscus, may be apparent
on either. Abdominal x-rays can also provide information about the pattern of
bowel gas (e.g., intestinal obstruction), edema and pneumatosis of the bowel
wall, retroperitoneal structures (e.g., pancreatic calcification), bony structures
(e.g., fractures, bone metastases).
More sophisticated diagnostic imaging is often valuable. Ultrasound is very
useful in the diagnosis of biliary tract, abdominal aortic, and gynecologic dis-
ease and is often used in suspected appendicitis. Increasingly, abdominal CT
scanning is being used for diagnosis of the acute abdomen, often obviating the
need for more invasive or uncomfortable studies. A contrast enema may be
obtained to show the level of a large bowel obstruction and to exclude pseu-
do-obstruction. Intravenous pyelography can demonstrate kidney nonfunction
or hydroureter in suspected renal pain. An opaque calculus may be seen on
plain abdominal x-rays. In suspected bowel ischemia, mesenteric angiography
may be used to confirm the diagnosis and evaluate therapeutic options. In sus-
pected diverticulitis, ultrasound and CT scanning will demonstrate diverticu-
la and thickening of the wall of the sigmoid colon, and evaluate the presence
of an associated abscess or gross perforation. The choice of investigation
should be discussed with a radiologist.
Laparoscopy has an important diagnostic role, as well as allowing defin-
itive surgical therapy (e.g., appendectomy, omental patch of a perforated
duodenal ulcer).

A reasonably specific diagnosis or focused differential can usually be estab-
lished early on and is the ideal basis for determining further management. In
some instances (e.g., possible appendicitis), careful observation with repeated
examination and selected imaging studies (e.g., ultrasound) allow a diagnosis
to be reached. In many individuals, acute abdominal pain of mild to moderate
severity resolves, at least in the short term, without a confirmed diagnosis.
In patients with more serious conditions, intravenous fluid administra-
tion, other supportive measures and monitoring must be instituted follow-
ing rapid initial assessment, even before a specific diagnosis can be made.
In such individuals, diagnostic and therapeutic maneuvers must proceed in
a coordinated and efficient manner. Occasionally, patients with an acute
abdomen, typically those who are unstable despite resuscitation or who
have obvious generalized peritonitis, require urgent laparotomy without a
definitive preoperative diagnosis.
13. CHRONIC ABDOMEN / W.G. Thompson
13.1 Synonyms
Recurrent abdominal pain; recurrent abdominal pain in children.
13.2 Description
Ten percent of children suffer recurrent abdominal pain and approximately
20% of adults have abdominal pain at least six times per year unrelated to men-
struation. The pain is chronic when it is continuous and has been present for
six months or more, unrelated to gastrointestinal functions such as eating and
defecation. It is often a feature of dyspepsia or the irritable bowel syndrome.
Characteristically, the pain has no relationship to bodily functions, and no gas-
trointestinal, hepatobiliary, genital or renal cause for the pain can be found.
13.3 Causes and Mechanism

The mechanisms of abdominal pain are discussed above, in Section 12
(“Acute Abdomen”). Of course, chronic abdominal pain may be caused by
many organic diseases. Peptic ulcer generally produces pain after meals or on
an empty stomach and is relieved by food or antacid. Abdominal pain awak-
ening the patient at night is a particularly discriminating feature. Peptic ulcers
are now more common in the elderly, especially women on NSAIDs. In them
the pain may be atypical.
Biliary colic may be due to cystic or common bile duct obstruction by a
stone. Characteristically this pain is significant enough to awaken the patient
at night or require a visit to the emergency room for analgesia. It lasts from
1 hour to 12 hours; beyond that time consider acute cholecystitis or pancre-
atitis. Attacks are sporadic and at intervals, not continuous. Biliary pain is
located in the epigastrium, the right upper quadrant and/or the right scapula.
It leaves the patient shaken but well. Should the gallbladder become inflamed,
cholecystitis results. Obstruction of the common bile duct with a stone results
in pain, jaundice and sometimes fever (cholangitis).
Pancreatitis is a devastating illness, with steady epigastric pain radiating to
the back and sometimes accompanied by shock. It almost always requires
admission to hospital.
Ischemic bowel disease, subacute bowel obstruction caused by Crohn’s dis-
ease, neoplasm or volvulus may present with recurrent bouts of abdominal
pain, often related to eating. These conditions are usually progressive and
accompanied by physical signs.
In a patient with diverticular disease, a peridiverticular abscess may devel-
op, causing recurrent bouts of severe left lower quadrant abdominal pain and
fever. Usually, diverticula are asymptomatic and symptoms that do occur are
those of coincident irritable bowel syndrome.
Renal colic due to a stone in the ureter is rarely chronic but may be recur-
rent. It consists of severe flank pain radiating to the groin and testicle, and
may be accompanied by hematuria. Typically, a patient smitten with renal
colic is unable to lie still.
Gynecologic conditions ranging from mittelschmerz (ruptured ovarian cyst)
to pelvic inflammatory disease may account for recurrent abdominal pain.
Menstruation-related pain in a young woman suggests endometriosis. Chron-
ic pelvic pain often relates to the irritable bowel syndrome.
Chronic appendicitis probably does not exist.
The chronic abdomen is seldom explained by the above mechanisms.
Functional abdominal pain may originate in any part of the gastrointestinal
tract or biliary tree. It is unrelated to bodily function and may be continuous.
The commonest cause of recurrent abdominal pain is the irritable bowel syn-
drome, in which there is a relationship to disordered defecation. It is uncertain
whether such pain is due to a normal perception of abnormal gut motility or
an abnormal perception of normal motility, or indeed if it is due to the gut at
all; there are frequently accompanying psychosocial difficulties.
13.4 Important Historical Points and Physical Examination Features

Pain, when related to a bodily function – defecation, eating, micturition or
menstruation – should focus the investigation upon the involved system.
Certain physical findings (such as an abdominal mass, or blood or mass upon
rectal examination) point to specific organic diseases. Fever, weight loss,
rectal bleeding and/or anemia indicate further tests. These features are absent
in chronic functional abdominal pain.
13.5 Differential Diagnosis, Diagnosis and Management

Management of the organic causes of the chronic abdomen can be directed
at the underlying disease process. In many instances, however, there is no
organic basis. Here, the physician’s responsibility is to reassure the patient
that no serious disease exists, and help the patient coexist with the symp-
toms in the light of the patient’s social background. One might improve
digestion through regular and better eating habits, and treat bowel dys-
function, particularly constipation, with increased dietary bulk.
13.6 Pain and Emotion

There are patients who have severe recurrent abdominal pain unrelated to bodily
function or organic disease. Such patients see many doctors without satisfaction;
the genesis of the symptom is thought to be psychogenic. This pain is often

given such descriptors as “illness behavior” and “pain proneness.” Some have
hypochondriasis and do not improve when organic disease has been
disproved. An extreme example is the Münchausen syndrome, where the
patient deliberately relates a tall tale of medical duress in order to precipitate
treatment, perhaps even surgery.
Functional pain is frequent in those who have recent conflicts, have experi-
enced a death in the family, or have become overly concerned with fatal ill-
ness. Depression and anxiety are frequent. Here, it is important not to carry
out extensive investigation in a fruitless search for an elusive cause. This only
reinforces the patient’s belief that something is wrong and undermines the
patient’s confidence in the benign diagnosis.
Such pain may be an emotional expression, in which case regular visits are
necessary to allow the patient to vent his or her problems. Drugs, especially
narcotics, should be used with restraint, and the physician should strive to
develop a strong doctor–patient relationship while dealing with the patient’s
depression, anxiety, frustration and often hostility. Some individuals benefit
from low-dose antidepressants, as in other chronic pain syndromes. These
patients test our skill in the art rather than the science of medicine.
14. JAUNDICE / L.J. Scully
14.1 Definition
A state characterized by increased serum bilirubin levels and a yellow appear-
ance due to deposition of bile pigment in the skin and mucus membranes.
14.2 Mechanism
Bilirubin is a waste product of hemoglobin metabolism. Interruption of the
breakdown pathway at any of a number of steps, or a marked increase in load
due to red cell destruction, results in an increase in serum bilirubin and (if
high enough) clinical jaundice.
Under normal circumstances senescent red blood cells are taken up and
destroyed in the reticuloendothelial system. Through a number of steps the
heme molecule of hemoglobin is converted to bilirubin and, tightly bound to
albumin, is transported in the plasma to the liver cells. Hepatocytes take up
bilirubin, conjugate it to glucuronide and excrete the bilirubin diglucuronide
in bile into the duodenum. In the bowel, bacteria break down bilirubin to uro-
bilinogen, 80% of which is excreted in the feces, contributing to the normal
stool color. The remaining 20% is reabsorbed and excreted in bile and urine
(enterohepatic circulation of urobilinogen).
Functional or anatomic obstruction at almost any level in this pathway

(from hemoglobin breakdown to uptake by the hepatocellular membrane to
excretion into the biliary system) will result in jaundice, with an increase in
serum bilirubin. A large increase in the breakdown products of hemoglobin
alone (e.g., hemolytic anemia) will cause an increase in serum unconjugated
bilirubin. If the problem lies after the uptake and conjugation step, the
increase is in serum conjugated bilirubin. Causes of jaundice are usually
classified as: (1) hemolysis; (2) genetic defects in bilirubin handling;
(3) hepatocellular disease; and (4) obstruction.
14.3 Clinical Presentation

Clinical jaundice is detected when the serum bilirubin level reaches 2–4 mg/dL
(40–80 µmol/L). It is usually preceded by a few days of pale stools (as excre-
tion of bilirubin into the intestine is decreased) and dark urine (due to
increased glomerular filtration of conjugated bilirubin). Jaundice is usually
first detected in the sclera, although the bilirubin is actually deposited in the
overlying conjunctival membranes. Yellow skin without scleral icterus should
suggest carotenemia or the ingestion of such drugs as quinacrine.
Most patients with jaundice, excluding those in whom it is secondary to
hemolysis, have nausea, anorexia and discomfort over the liver. There may be
hepatomegaly, masses in the epigastrium or pancreas or a dilated gallbladder.
Signs of chronic liver disease such as spider nevi or palmar erythema are
important. Pruritus may result, presumably from the deposition of bile salts
(or a retained pruritogen normally excreted in bile) in the skin.
Several genetic defects in the conjugation or excretion of bilirubin may
cause long-standing unconjugated or conjugated hyperbilirubinemia.

Initially the most important information is whether the jaundice is due to
conjugated or unconjugated hyperbilirubinemia (Figure 2). Serum bilirubin
can be fractionated from “total” into conjugated and unconjugated, but the
presence of bile in the urine determined by a test strip at the bedside confirms
that the bilirubin rise is predominantly in the conjugated form. If the bilirubin
is unconjugated, hemolysis or genetic defects are implicated. If the bilirubin
is conjugated, “liver biochemical tests” (AST, ALT, GGT and alkaline phos-
phatase) will help determine if the jaundice is primarily due to obstruction/
cholestasis (high GGT and alkaline phosphatase) or hepatocellular damage
(high AST and ALT). Cholestatic jaundice requires ultrasound as the best, first
test to detect biliary tract disease. If the jaundice is cholestatic, then an ultra-
sound of the abdomen is required to determine if there is obstruction of the
ducts or intrahepatic bile duct dilation.
FIGURE 2. Causes of hyperbilirubinemia.
14.5 Management
The management of obstructive jaundice is directed toward the cause where
possible (e.g., removal of obstructing gallstone). Jaundice secondary to hepato-
cellular disease, such as viral hepatitis, does not require any specific treat-
ment. Jaundice due to alcohol, toxin or drug requires withdrawal of the
offending agent.
15. ASCITES IN CHRONIC LIVER DISEASE / L.J. Scully
15.1 Definition
Ascites is the accumulation of nonsanguinous fluid in the peritoneal cavity.
15.2 Mechanisms
With significant liver disease, albumin synthesis is reduced. Low serum
albumin results in a decrease in intravascular osmotic pressure. This causes
renal blood flow changes, resulting in sodium and water retention. Increased
aldosterone levels, possibly due to decreased catabolism of this hormone by
the liver, also contribute. There is a generalized salt and water retention, but
the fluid accumulation may be confined to the peritoneal cavity or may be
associated with peripheral edema. Ascites develops because of increased
portal pressure and the transudation of fluid from the capillaries in the portal
system to the peritoneal cavity. Hepatic lymph production also increases and
extravasates directly into the peritoneal cavity.
15.3 Signs and Symptoms

Ascites most commonly presents with increasing abdominal girth, often asso-
ciated with an uncomfortable feeling of distention, and sometimes nausea and
anorexia. Shortness of breath may develop, resulting from either elevation of
the diaphragm or pleural effusion. Ankle edema may accompany ascites.
Clinical examination reveals flank fullness on inspection. “Shifting dullness”
or a “fluid thrill” may be elicited. Smaller amounts of fluid may be detected on
ultrasound when clinical signs are absent. One should look for other signs of por-
tal hypertension, such as dilated abdominal wall veins or an enlarged spleen.

Newly developed ascites must have a diagnostic aspiration to determine the
albumin level, cell count and cytology. The fluid should be clear and straw-
colored. Occasionally, lymph can accumulate in the peritoneal cavity, causing
“chylous ascites,” which requires different management. Ascitic fluid may
become infected, in which case the white blood cell count will be elevated in
the fluid. If the fluid is sanguinous, other causes – such as infection or malig-
nancy – must be sought. The serum ascites albumin gradient is the best way
of confirming if the ascitic fluid is secondary to portal hypertension. In this
situation the gradient is high (i.e., > 11 g/L) whereas it is low if the ascites is
due to peritoneal carcinomatosis. This is far more accurate than our previous
assessment of transudative versus exudative ascites.

Management initially includes bed rest and salt restriction. Most cases also
require adding a diuretic such as spironolactone. Careful aspiration of large
quantities (up to 8 L) of ascitic fluid may be necessary in some resistant cases;
this can be safely performed, and if the serum albumin level is very low an
intravenous infusion of albumin is given before the paracentesis.
16. GASTROINTESTINAL BLEEDING / A. Rostom and C. Dubé
16.1 Description
Gastrointestinal (GI) bleeding may be referred to as upper, lower, obscure
or occult.
Upper GI bleeding commonly presents with hematemesis (vomiting of
blood or coffee-ground like material) and/or melena (black, tarry stools).
The physical aspect of melena is the result of degradation of blood by
intestinal bacteria. In comparison, hematochezia (bright red or maroon
colored blood or fresh clots per rectum) is usually a sign of lower GI bleed-
ing. Lower GI bleeding is usually defined as bleeding distal to the ligament
TABLE 3. The important causes of upper GI bleeding
Acute bleeding
Peptic ulcer disease: duodenal ulcer, gastric ulcer, stress erosions
Esophagitis: peptic esophagitis, pill esophagitis, infectious
Portal hypertension-related: gastro-esophageal varices, portal hypertensive gastropathy
Neoplastic: esophageal cancer, gastric cancer, lymphoma, metastatic cancer
Vascular: angiodysplasia, Dieulafoy lesion, radiation-induced
Traumatic: Mallory-Weiss tear, aorto-enteric fistula, foreign body ingestion
Miscellaneous: hemobilia, hemosuccus pancreaticus
Chronic bleeding
Esophagitis
Potal hypertensive gastropathy
Malignancies
Angiodysplasia
Radiation
Inflammatory bowel disease
of Treitz. However this definition can cause confusion since proximal small
bowel bleeds tend to be associated with elevated levels of blood urea
nitrogen (BUN) which is classically associated with upper GI bleeding.
Alternatively the location of GI bleeding can be defined as upper – above
ligament of Treitz, small bowel – ligament of Treitz to distal ileum, and
lower – terminal ileum and colon.
Occult bleeding is defined as the initial presentation of a positive fecal
occult blood test (FOBT) result and/or iron-deficiency anemia (IDA), when
there is no evidence of visible blood loss to the patient or physician. Obscure
bleeding is defined as bleeding of unknown origin that persists or recurs
after a negative initial or primary endoscopy (colonoscopy and/or upper
endoscopy) result. Obscure bleeding may be so-called “obscure-overt,”
(i.e., clinically manifest such as melena or hematochezia), or may be
“obscure-occult,” such as persistent IDA.
The important causes of upper and lower GI bleeding are presented in
Tables 3 and 4 respectively.

The initial evaluation of the patient with upper GI bleeding involves early
assessment of the “ABCs.” Patients with upper GI bleeding are at risk of air-
way compromise from aspiration of vomited blood and/or from reduced level
TABLE 4. The important causes of lower GI bleeding
Acute bleeding
Diverticulosis
Angiodysplasia
Ischemic colitis
Colonic malignancy
Radiation-induced
Infectious enteritis or colitis
Solitary rectal ulcer syndrome
Post-polypectomy
Hemorrhoids
Chronic bleeding
Angiodysplasia
Colonic malignancy
Radiation-induced
Hemorrhoids
of consciousness due to shock or hepatic encephalopathy. Early assessment of

the airway and breathing is crucial; some patients may require supplemental
oxygen or even intubation for airway protection and/or assisted breathing.
During the early assessment of the hemodynamic status, two large bore
peripheral IVs (18 gauge or greater) are placed for fluid and blood product
restoration, and their early placement allows for the simultaneous drawing of
blood for urgent blood typing and cross-matching, and measurement of the
blood count, coagulation parameters, electrolyte and renal function as well as
albumin and liver enzymes as clinically indicated.
In chronic or recurrent bleeding, either occult or clinically manifest, symp-
toms are most often related to iron deficiency and anemia: pallor, fatigue,
dyspnea and, in a predisposed individual, congestive heart failure or angina.
In acute GI bleeding, the symptoms associated with blood loss, such as weak-
ness, diaphoresis, pre-syncope, and syncope, may occur before any blood appears
externally. Blood passage through the intestines acts as a cathartic, so that hyper-
peristalsis may be present and bowel frequency is increased. The pigmentation of
the stool will depend on the rate of bleeding as well as the length of time in tran-
sit along the bowel: stools can vary from a deep black tarry aspect to a dark
burgundy or to a bright red color. In determining the likely source of bleeding, the
clinician needs to interpret the patient’s manifestations of bleeding in conjunction
with the hemodynamic status. Blood originating from the left colon typically is
bright red. However, hematochezia associated with resting tachycardia and/or
hypotension raises the suspicion of a brisk upper GI bleed; similarly, while the
passage of black tarry stools is most commonly associated with an upper GI
source, dark burgundy or black stools can sometimes be encountered in proximal
colonic bleeds. In the absence of spontaneous passage of stools, a digital rectal
examination to determine the stool color will be most informative.
Hematemesis, when present, may be apparent as bright red blood, with or
without clots, or of a dark brown and granular appearance, so-called coffee-
grounds. Bright red emesis is suggestive of an esophageal source of bleed or
of a brisk upper GI source. Bleeding into the duodenum may or may not reflux
into the stomach, therefore the absence of hematemesis or of a bloody aspi-
rate from nasogastric suction does not rule out that condition.
Under certain circumstances it may be difficult to determine if the GI bleed,
particularly if it is significant, is of upper or lower origin. It is then safest to
initially proceed on the assumption of an upper GI bleed, and to arrange for
early upper endoscopy after initial resuscitation. Upper endoscopy is quick to
perform, allows relatively easier endoscopic treatment of potentially serious
causes of bleeding, and if negative, little time has been wasted. Furthermore,
a negative upper endoscopy in the setting of ongoing rapid GI bleeding assists
the angiographer, by clearing the celiac axis and allowing them to concentrate
on the superior and inferior mesenteric arteries.
On history, information should be gathered about medication use, in partic-
ular the intake of NSAIDs or anticoagulants, prior history of peptic ulcer dis-
ease, history of abdominal surgery (e.g., gastric surgery raises the suspicion of
prior peptic ulcer disease or carcinoma, bowel resection may reduce the transit
time of blood through the gut leading to atypical presentations, vascular grafts
raise the suspicion of aorto-enteric fistulas), history of chronic liver disease or
alcohol abuse which might also be supported by suggestive physical signs.
The hemodynamic status should be interpreted in light of the patient’s
abilities to compensate for hypovolemia: in a young and fit adult, the presence
of a resting or orthostatic tachycardia should be interpreted as a sign of signifi-
cant volume loss, while the loss of an equivalent blood volume in an elderly or
debilitated subject would more likely be manifested by hypotension or shock.
Initial investigations include a complete blood count (CBC), red cell indices,
partial thromboplastin time (PTT) and international normalized ratio (INR), as
well as urea and creatinine. It is important to remember that, acutely, the hemo-
globin (Hb) and hematocrit (Ht) may not be reduced from normal, since these
measures reflect the red blood cell (RBC) concentration in the blood. Over the
ensuing 36–48 hours, most of the volume deficit will be repaired by the move-
ment of fluid from the extravascular into the intravascular space. Only at these
later times will the Hb and Ht reflect the true degree of blood loss. Further-
more, if a patient presents with an acute GI bleed and the initial Hb is low, one
should expect that the actual Hb is even lower than that measured, so that
early blood transfusion would be advisable in such cases. Some patients, in
particular those with GI malignancies, may have had chronic occult bleeding
prior to their acute presentation, in which cases hypochromia and microcytosis
from iron deficiency may be observed. Coagulopathy, either iatrogenic or
secondary to liver failure, should be addressed and corrected as clinically
indicated. An elevated blood urea nitrogen (BUN) value in the presence of a
normal creatinine may result from an upper GI bleed with hypovolemia.
Patients should be categorized as either low or high risk for complications
based upon their clinical presentation and hemodynamic status.
In upper GI bleeding, clinical predictors of mortality are: age older than
60 years, shock, poor overall health status, comorbid illnesses (coronary
artery disease, renal failure, sepsis and/or onset of bleeding while hospitalized
for another reason), presence of fresh red blood on rectal examination, in the
emesis or in the nasogastric aspirate, as well as continued bleeding or rebleed-
ing. In such cases, early endoscopy with risk classification by clinical and
endoscopic criteria allows for safe and prompt discharge of patients classified
as low risk, improves outcomes of patients classified as high risk and reduces
resource utilization for patients classified as either low or high risk. In peptic
ulcer bleeding, endoscopic criteria of rebleeding include active bleeding, a
visible vessel, or adherent clot. Early administration of intravenous proton
pump inhibitors, in conjunction with endoscopic therapy, is beneficial in such
cases. In variceal bleeding, intravenous administration of somatostatin
analogs and endoscopic therapy are also beneficial.
In lower GI bleeding, patients who have been successfully resuscitated
should undergo bowel cleansing followed by colonoscopy. If these procedures
are not feasible due to ongoing hemodynamic instability, arteriography and
surgical consultation should be obtained.
17. ABDOMINAL MASS / S. Grégoire
17.1 Description
When an abdominal mass is discovered on physical examination, one must
define its nature. Using a systematic approach often permits the identification
of the mass before the use of sophisticated tests.
17.2 Important Points in History and Physical Examination

Important clues in the history and general physical examination may help to
identify the enlarged viscus. For example, in a young patient presenting with
diarrhea, weight loss and abdominal pain, finding a right lower quadrant mass
would suggest inflammatory bowel disease. However, an abdominal mass
may be discovered during physical examination of an asymptomatic individ-
ual. Certain observations made during the abdominal examination may be
helpful (See also Section 19).
17.2.1 INSPECTION
Where is the mass located? A practical approach is to divide the abdomen into
four quadrants (See Section 19.1). Starting from the principle that an abdominal
mass originates from an organ, surface anatomy may suggest which one is
enlarged. A mass seen in the left lower quadrant, for example, could be of colonic
or ovarian origin but, unless there is situs inversus, one would not consider an
appendiceal abscess.
Does the mass move with respiration? In the upper abdomen a mobile intra-
abdominal mass will move downward with inspiration, while a more fixed
organ (e.g., aorta, pancreas) or an abdominal wall mass (e.g., hematoma of
rectus muscle) will not.
Is there visible peristalsis?
17.2.2 AUSCULTATION
Careful auscultation for bowel sounds, bruit or rub over an abdominal mass is
part of the systematic approach.
17.2.3 DEFINING THE CONTOUR AND SURFACE OF THE MASS

This is achieved by inspection, percussion and palpation. Is the organ air-
filled (e.g., stomach) or fluid-filled? Is it a well-defined mass (e.g., liver,
spleen) or are its borders difficult to define (matted loops of small bowel)? Is
the surface regular? An enlarged liver due to fatty infiltration may have a
smooth surface, while a cirrhotic organ is usually irregular and nodular. What
is the consistency of the mass? Firm? Hard or soft? Is it pulsatile? In the
absence of ascites, ballottement of an organ situated in either upper quadrant
more likely identifies an enlarged kidney (more posterior structure) than
hepatomegaly or splenomegaly.

The following suggests an approach to the differential diagnosis of an abdom-
inal mass located in each quadrant:
17.3.1 RIGHT UPPER QUADRANT

This location suggests liver, right kidney, gallbladder and, less commonly, a
colon or gastroduodenal mass. A pancreatic mass is rarely palpable.
17.3.1.1 Liver
As a subdiaphragmatic organ, the liver moves downward with inspiration.
This anterior organ has an easily palpable lower border, which permits
assessment of its consistency. A bruit or venous hum can be heard in certain
conditions. An enlarged left lobe can usually be felt in the epigastric area.
17.3.1.2 Right kidney

The kidney may protrude anteriorly when enlarged and be difficult to differen-
tiate from a Riedel’s lobe of the liver. It may be balloted.
17.3.1.3 Gallbladder
This oval-shaped organ moves downward with inspiration and is usually
smooth and regular.
17.3.1.4 Colon
Colon masses are deep and ill-defined, and do not move with respiration.
High-pitched bowel sounds suggest obstruction.
17.3.2 LEFT UPPER QUADRANT

Location in the left upper quadrant suggests spleen or left kidney. Less com-
monly, a colonic (splenic flexure) or gastric mass can be felt. A pancreatic
mass is rarely palpable.
17.3.2.1 Spleen
This anterior organ moves downward with inspiration. Since it has an oblique
longitudinal axis, it extends toward the right lower quadrant when enlarged. It
has a medial notch and the edge is sharp.
17.3.2.2 Left kidney

Its more posterior position and the presence of ballottement helps distinguish
the left kidney from the spleen.
17.3.2.3 Colon, pancreas, stomach

It is practically impossible to differentiate masses in these organs by physical
examination. The history helps but often one must resort to radiology or endoscopy.
17.3.3 RIGHT LOWER QUADRANT

A mass in this area has its origin either in the lower GI tract (colon, distal
small bowel, appendix) or in a pelvic structure (ovary, uterus, fallopian tube).
17.3.3.1 Lower GI tract

These deeper organs are usually ill-defined. Clinical context is important.
Inflammatory bowel disease usually would be associated with pain on palpa-
tion but carcinoma of the cecum would be painless.
17.3.3.2 Pelvic organs

Bimanual palpation is the preferred method.
17.3.4 LEFT LOWER QUADRANT

As with a right lower quadrant mass, the differential diagnosis here is between
lower GI (in this quadrant the sigmoid colon) and pelvic origin. The shape of
the organ and pelvic examination should help differentiate the two.

To complete the assessment of an abdominal mass, one may choose among
several different investigational tools. The use of specific tests depends on
availability and on the organ studied.
Generally, ultrasound is useful. This noninvasive, safe, cheap and widely
available method identifies the mass and provides information on its origin
and nature. Ultrasound may also be used to direct a biopsy. Other noninvasive
modalities are nuclear imaging and CT scan. Hollow organs may be demon-
strated radiographically through the use of contrast media (e.g., barium
enema, GI series, ultrasound, intravenous pyelogram, endoscopic retrograde
cholangiopancreatography, etc.). Sometimes, laparotomy or laparoscopy will
be necessary to make the diagnosis.
18. PROCTALGIA FUGAX / W.G. Thompson

18.1 Description
Proctalgia fugax is a sudden severe pain in the anus lasting several seconds or
minutes and then disappearing completely.
18.2 Mechanism
The pathophysiology of proctalgia fugax is uncertain. Although some obser-
vations (under obviously fortuitous circumstances) suggest a rectal motility
disorder, the symptom appears more likely to result from spasm of the skele-
tal muscle of the pelvic floor (specifically, the puborectalis).
18.3 History and Physical Examination

Proctalgia fugax occurs in about 14% of adults and is somewhat more com-
mon in females than males. The pain may be excruciating, but since it is so
short-lived patients seldom report it to their physician. In 90% of instances it

lasts less than five minutes and in many cases less than a minute. About one-
third of patients suffer attacks following defecation. A small minority report
attacks following sexual activity. There are no physical signs.

Perianal disease may cause pain but it usually accompanies, rather than fol-
lows, defecation. One should be particularly careful to exclude the presence
of an anal fissure, which may be difficult to see on anal inspection. Pain
originating from the coccyx may be accompanied by coccygeal tenderness
both externally and from within the rectum. An acute attack of anal pain last-
ing several hours may indicate a thrombosed hemorrhoid. However, constant
pain for many months or years is not likely to be proctalgia fugax or to have
an organic explanation.
18.5 Management
Beyond reassurance there is no treatment.
19. EXAMINATION OF THE ABDOMEN / R.F. Bursey, J.M. Fardy,

D.G. MacIntosh and N. Saloojee
Examination of the abdomen is an important component of the clinical assess-

ment of anyone presenting with suspected disease of the gastrointestinal tract.
As in all other parts of the examination, care must be taken to show respect and
concern for the patient while ensuring an appropriate and thorough examination.
While performing the examination it is useful to keep in mind the concepts
of sensitivity and specificity. How confident can we be that a suspected phys-
ical finding is in fact present and has clinical significance? For example, how
sensitive and specific is our bedside examination for hepatomegaly? What is
the clinical significance of an epigastric bruit heard in a thin 20-year-old
female versus a 55-year-old hypertensive, obese male?
In the following sections we will describe an appropriate sequential examina-
tion of the abdomen and highlight some of the potential pitfalls of this process.
19.1 Inspection
Start from the usual position to the right side of the patient. Ensure that the
abdomen is exposed from the costal margin to symphysis pubis. When
describing the location of an abnormality it is useful to divide the abdomen
into four quadrants with a perpendicular line through the umbilicus from the
xiphoid process to the symphysis pubis. A horizontal line through the umbilicus
FIGURE 3. Division of the abdomen into four quadrants: the left upper quadrant, right upper
quadrant, left lower quadrant and right lower quadrant.
then allows the abdomen to be divided into 4 areas: the left upper, right upper,
left lower and right lower quadrants (Figure 3). On occasion it may be helpful
to divide the abdomen into 9 regions with the spaces marked by vertical lines
through the left and right mid-clavicular lines and horizontal lines passing
through the subcostal margins and anterior iliac crests (Figure 4).
The overall appearance such as scaphoid, protruberant, or obese should be
described, and the location of any surgical scars noted. One should look for any
abnormal surface markings, including cutaneous lesions as well as vascular
markings. Note any pulsation. A comment should also be made about the
apparent ease of movement of the abdominal wall with respiration and change
in body position. Normally the abdominal wall will rise with inspiration. Occa-
sionally organomegaly or a mass will be visible. It is helpful to look at the
abdomen from the foot of the bed as well.
19.2 Auscultation
It is useful to auscultate the abdomen prior to palpation or percussion, as
bowel sounds induced by further examination may mask vascular bruits or
pleural rubs. When listening for vascular bruits it is useful to keep in mind
FIGURE 4. Division of the abdomen into nine regions.
the surface markings. The aorta enters the abdomen at or just to the left of the
xiphoid process and bifurcates to the left and right common iliac arteries at
the level of the umbilicus. The renal arteries are found approximately one-
half the distance between the xiphoid process and the umbilicus, and auscul-
tation is best performed within 2 cm of the midline. Bruits are often best
heard at the bifurcation of major vessels; therefore it is also appropriate to
listen at the bifurcation of the common iliacs into the internal and external
iliacs, approximately halfway between the umbilicus and the inguinal liga-
ment. One should listen over the inguinal ligament for femoral bruits as well.
A venous hum is best heard overlying the portal vein, which is found in an
area approximated by an elliptical shape between the umbilicus and the mid-
clavicular line where it crosses the right subcostal margin. Arterial bruits are
usually heard only during systole and best heard with the diaphragm of the
stethoscope, as they are high pitched. A venous hum is more likely to be
continuous and best heard with the bell of the stethoscope, as this is a low-
pitched sound. There are, however, no studies to suggest these findings are
helpful or reliable in routine examination. Venous hum can occur in portal
venous hypertension of any cause. Undifferentiated liver patients in one study
had a prevalence of bruits reported as less than 3%. The ability of clinicians
to distinguish hepatic arterial bruits from other arterial bruits such as a renal
artery bruit has not been studied.
Friction rubs may occur overlying the liver or spleen and are always abnor-
mal, though rare. Even with careful auscultation of patients with known liver
tumors, fewer than 10% are found to have a rub.
19.2.1 BOWEL SOUNDS

Auscultation for bowel sounds is a rather controversial subject. Bowel sounds
should be listened for prior to palpation or percussion, but the yield of this
examination is low. The diaphragm of the stethoscope should be placed on the
abdomen, as least initially in the right lower quadrant near the ileocecal valve.
The particular characteristics of the bowel sounds or even absence of them is
not diagnostic of a particular condition, perhaps except for the very high
pitched noises of acute small bowel obstruction. Complete absence of bowel
sounds may indicate an ileus or peritonitis.
19.3 Palpation
Palpation of the abdomen should be done in an orderly sequence with the
patient in the supine position. Light palpation should be done first in all four
quadrants assessing for areas of potential tenderness. Light palpation is a one-
handed technique. With the pads of the fingertips, palpate in a gentle, circular
motion. If no areas of obvious tenderness are elicited, then deep palpation is
performed, again in all four quadrants using a two-handed technique. Pressure
is applied with one hand over the other hand, which is placed on the abdomi-
nal wall, as it is thought that deep palpation with one hand may lead to the
inadvertent nonrecognition of suble fullness or mass if the hand applying deep
pressure is also responsible for detecting the abnormality. The accuracy of this
is untested. It is stated that if a patient has difficulty relaxing the abdominal
wall musculature, then placing the soles of the patient’s feet on the bed with
hips and knees flexed will aid relaxation; in all likelihood, however, a calm,
organized approach with verbal reassurance by the examiner will be just as
effective. Assess for peritoneal irritation in each quadrant by checking for
rebound tenderness. Press the fingertips in slowly and firmly. Quickly with-
draw them. If withdrawal elicits pain, this suggests peritoneal irritation.
The techniques of palpation of liver and spleen are discussed in Sections
19.5 and 19.6.
19.4 Percussion
Percussion of the abdomen will detect the presence of bowel gas. The tech-
nique as it relates to defining organomegaly and the presence of fluid is dis-
cussed in later sections.
19.5 Examination of the Liver

Examination of the liver consists mainly of palpation for the lower edge of the
liver and percussion to determine the span. This examination is performed
after inspection for right upper quadrant swelling and extrahepatic signs of
liver disease. To palpate the lower edge of the liver the examiner starts with
gentle pressure in the right lower quadrant of the abdomen. The edge of an
enlarged liver may be missed by starting too high in the abdomen. The patient
is asked to breathe gently and slowly, in order to bring the liver edge down to
the examining fingertips of the right hand. The examiner moves the right hand
in a cephalad direction about 2 cm with each breath. If the edge is not felt, no
further examination is required. If liver disease is suspected the lower liver
edge can be located by percussion.
If the edge is located, mark the lower border in the mid-clavicular line. Per-
cuss for the upper border starting in the third intercostal space with a finger
that is held flat and lies within the space. Move down one interspace at a time
until the percussion note changes from resonant to dull. To confirm the change
of percussion note strike the third and fourth fingers laid in adjacent inter-
spaces. The note on the top finger should be resonant and on the lower dull.
Measure the distance between the upper and lower percussion edges in the
mid-clavicular line. Determination of the liver span can be done with firm or
gentle percussion to locate the lower border. Gentle percussion is the recom-
mended technique, as this method appears to better estimate liver span as
judged by ultrasound. Remember that the upper edge of the liver is dome
shaped and not straight across.
The scratch test has been used to find the lower liver margin. The
diaphragm of the stethoscope is placed at the right costal margin in the mid-
clavicular line. A finger moves up the abdomen in the mid-clavicular line,
scratching gently and with consistent pressure. When the liver edge is
reached, there is a sudden increase in the scratching sound heard through the
stethoscope. In one comparative study the scratch test was not felt to offer any
advantage over the techniques of palpation and percussion.
When the liver edge is palpable, trace the edge working laterally to medi-
ally. Try to determine the characteristics of its surface – for example, soft, firm
or nodular. These characteristics may help in the assessment of patients with
liver disease; however, agreement about the characteristics is poor, even
among experts. Auscultation is rarely helpful. An attempt should be made to
assess the left lobe in the epigastrium using these techniques.
What is the significance of a palpable liver edge? A recent review suggest-
ed that a palpable liver is not necessarily enlarged or diseased. When clinical
examination is compared to nuclear medicine scanning, about one-half of pal-
pable livers are not enlarged. The inability to feel a liver edge does not rule
out hepatomegaly, but does reduce its likelihood.
What is the normal percussion span? Only one study has been done to
establish the normal span. Castell examined 116 healthy subjects using firm
percussion. The mean span in the mid-clavicular line was 7 cm in women and
10.5 cm in men. The following nomograms were developed to predict
estimated liver dullness in a normal population using firm percussion tech-
nique: Male liver dullness equals (0.032 X weight in pounds) + (0.183 X
height in inches) – 7.86. The female liver dullness equals (0.027 X weight in
pounds) + (0.22 X height in inches) – 10.75. The 95% confidence intervals
were ±2.64 cm. Therefore a 5 ft. 10 in., 175 lb. male would have an estimat-
ed liver span of 10.2 cm (range 7.6–12.8) and a 5 ft. 5 in., 130 lb. female
would have an estimated liver span of 7.1 cm (4.5–9.7 cm) by this formula.
19.6 Examination of the Spleen

The normal spleen is a curved, wedge-shaped organ located beneath the rib
cage in the upper left quadrant. The spleen lies beneath the left tenth rib and
normally weighs about 150 g, measuring approximately 12 cm in length, 7 cm
in width and 3 cm in thickness. The normal spleen usually cannot be palpat-
ed, but as it enlarges it descends below the rib cage, across the abdomen
toward the right lower quadrant. An enlarged spleen may have a palpable
notch along its medial edge.
Examination of the spleen should begin with observation of the left upper
quadrant for an obvious mass, though such a mass is quite uncommon. The
examiner should then proceed with percussion over the area of the spleen to
look for evidence of dullness, implying splenic enlargement. The two most
useful methods are percussion over Traube’s space and Castell’s sign.
The surface markings for Traube’s space are the left sixth rib, the left mid-
axillary line and the left costal margin. An enlarged spleen may cause dullness
over Traube’s space. Percussion should be carried out at one or more levels
of Traube’s space from medial to lateral. This maneuver has a sensitivity and
specificity between 60 and 70% for splenic enlargement; however, the
sensitivity and specificity increases to approximately 80% in non-obese
patients who are fasting.
Castell’s method involves percussion in the lowest intercostal space in the
left anterior axillary line. In normal individuals this area is resonant on per-
cussion and remains resonant on inspiration. In patients with mild splenic
enlargement this area will be resonant on percussion and become dull on max-
imal inspiration. This method has a sensitivity and specificity of approximate-
ly 80% for detection of splenic enlargement and would seem particularly suit-
ed for detection of a minimally enlarged spleen that may not be palpable.
Palpation of the spleen should begin in the right lower quadrant and pro-
ceed toward the left upper quadrant in order to follow the path of splenic
enlargement. Palpation should initially be carried out in the supine position

with a bimanual technique using the left hand to gently lift the lowermost por-
tion of the left rib cage anteriorly. The fingertips of the right hand are used to
palpate gently for the spleen tip on inspiration. The hand is moved from the
right lower quadrant, advancing toward the left upper quadrant. If the spleen is
not palpated in the supine position the patient should be moved into the right lat-
eral decubitus position and again with bimanual technique the spleen tip should
be sought using the fingertips of the right hand on inspiration. This technique has
a sensitivity of about 70% and specificity of 90% for splenic enlargement.
19.7 Examination for Suspected Ascites

The presence of ascites – free fluid within the abdominal cavity – is always
due to an underlying pathological process. Most often the underlying
etiology is cirrhosis of any type. Other potential causes include severe
right-sided heart failure, lymphatic obstruction, primary intra-abdominal
malignancy and peritoneal metastases. It is easy to identify large-volume
ascites clinically, but the sensitivity of the examination techniques falls
with lower volumes of fluid. Ultrasound, which can detect as little as
100 mL of free fluid, is the gold standard against which the clinical diagnostic
maneuvers are compared.
An approach involves inspection for bulging flanks, followed by palpation for
the presence or absence of fluid waves combined with percussion to demonstrate
flank dullness as well as shifting dullness. One has to be aware that adipose
tissue in the flanks may be occasionally mistaken for free fluid. To demonstrate
a fluid wave it is necessary to enlist the aid of the patient or another individual.
With the patient in the supine position, place one hand on the patient’s flank.
With the other hand briskly tap the other flank. A third hand is placed in the mid-
abdomen with sufficient pressure applied to dampen any wave that may pass
through adipose tissue in the anterior abdominal wall. If fluid is present a shock
wave will be felt with the palpating hand. The sensitivity of this technique is
approximately 50% but it has a specificity of greater than 80%.
When percussing for free fluid one should place the finger parallel to the
expected edge and percuss from resonance in the mid-abdomen to dullness in
the flanks. This area is then marked and the patient rolled to the opposite side.
For example, if flank dullness is demonstrated on the left then the patient
should be rolled onto the right side. One should allow approximately 30 sec-
onds for the fluid to move between the mesentery and loops of bowel into the
inferior portion of the abdomen. The previous area of dullness in the left flank
should now be resonant. It does not matter which side one chooses to start
with. In three separate studies shifting dullness had a sensitivity that ranged
from 60–88% and a specificity that ranged from 56–90%.
In one study involving six gastroenterologists and 50 hospitalized alcoholic

patients, the overall agreement was 75% for the presence or absence of ascites
and reached 95% among senior physicians.
Interestingly, symptoms are often as useful as physical examination tech-
niques for the clinical diagnosis of ascites. The most useful findings to make
a diagnosis of ascites are a positive fluid wave, shifting dullness or peripher-
al edema. The absence of these findings is useful in ruling out ascites, as is a
negative history of ankle swelling or increasing abdominal girth.
SUGGESTED READING LIST
Section 19 Examination of the Abdomen

Castell DO, O’Brien KD, Muench H, Chalmers TC. Estimation of liver size by
percussion in normal individuals. Ann Intern Med 1969; 70(6):1183–1189.
Grover SA, Barkun AN, Sackett DL. Does this patient have splenomegaly? JAMA
1993; 270:2218–2221.
Naylor CD. Physical examination of the liver. JAMA 1994; 271:1859–1865.
Sapira JD. The art and science of bedside teaching. In: Sapira JD (ed.), The art and
science of bedside diagnosis. Baltimore: Urban & Schwarzenberg, 1990.
Williams JW, Jr, Simel DL. Does this patient have ascites? How to divine fluid in the
abdomen. JAMA 1992; 267:2645–2648.
Practice points
• Gastrointestinal complaints are common in the general population.

• Stress factors and fears of underlying malignancies are important triggers
for complaints to be brought to medical attention.
• Thorough and careful history-taking is crucial in gastroenterology and no
amount of endoscopic and radiologic investigations can replace it as a
diagnostic tool.
• Interpretation of the clinical manifestations of gastrointestinal disorders
requires a sound knowledge and understanding of gastrointestinal physiology.
• Gastrointestinal symptoms should be interpreted in light of their relation
to diet, food ingestion, digestion and defecation.
• Symptoms and signs such as weight loss, gastrointestinal bleeding, jaundice
or anemia should alert the clinician to the possibility of underlying organic
conditions and warrant investigations.
• Family history is an important part of the anamnesis; in particular, a family
history of bowel cancer, gastric cancer, celiac disease or hemochromatosis
should prompt screening tests as clinically appropriate.

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1

Common Symptoms and

With sections authored by:

1. INTRODUCTION / W.G. Thompson and C. Dubé

The key to accurate diagnosis and effective management of gastrointestinal

such phenomena as anemia, fever or incapacity to work may indicate a more

2. GLOBUS / C. Dubé and W.G. Thompson

2.5 Differential Diagnosis and Management

3. HEARTBURN AND REGURGITATION / C. Dubé and W.G. Thompson

4. DYSPHAGIA / A.S.C. Sekar

4.2 Important Historical Points and Differential Diagnosis

4.3 Approach to Diagnosis and Management

medically with nitroglycerin or calcium channel blocking agents. Achalasia and

5.3 History and Physical Examination

occurrence of dyspepsia. Indeed, dyspeptic symptoms are equally common in

5.4 Approach to Diagnosis and Management

6. NAUSEA AND VOMITING / M.C. Champion

6.3 Mechanism (Figure 1)

6.4 History and Physical

6.5 Differential Diagnosis

of nausea and vomiting, including intracerebral problems (e.g., hydrocephalus,

6.6 Approach to Diagnosis and Management

Phenothiazines also exert their action on the chemoreceptor trigger zone.

7. ANOREXIA / M.C. Champion

7.3 History and Physical

7.4 Differential Diagnosis

7.5 Approach to Investigation and Management

8. GAS AND BLOATING / W.G. Thompson

8.1 Synonyms and Related Terms

8.2 Farting, Gas, Wind, Flatus

8.3.2 CLINICAL MANIFESTATIONS OF AEROPHAGIA

8.4 Functional Abdominal Bloating

8.4.2 CLINICAL FEATURES

8.4.3 DIFFERENTIAL DIAGNOSIS

9. CONSTIPATION / C. Dubé and W.G. Thompson

TABLE 1. Some causes of chronic constipation

Primary diseases of the colon Pharmacologic

Pelvic floor dyssynergia Neurologic and muscular disorders

neurologic (multiple sclerosis, Parkinson’s disease), muscular (systemic scle-

9.4 Important Points on History and Physical

alternation of diarrhea with constipation should be enquired about. History

9.5 Approach to Diagnosis

9.6 Approach to Management

10. DIARRHEA / W.G. Thompson

10.4 Important Historical Points and Physical Examination Features

TABLE 2. Anatomic approach to the causes of chronic diarrhea

pets. Contaminated water may result in giardiasis, amebiasis or cryptococcosis.

10.5 Differential Diagnosis and Management

11. MALNUTRITION / D.G. Patel

1. Lack of food intake due to anorexia or food-related symptoms such as

11.3 Signs of Malnutrition

1. Weight loss in the absence of edema is a good indicator of energy deficiency.

12. ACUTE ABDOMEN / J.M. Watters

the groin accompanying ureteric obstruction. However, when the viability

12.4 Associated Symptoms

12.5 Physical Examination

contraction of initially relaxed muscles of the abdominal wall in response to

12.6 Differential Diagnosis

Serum amylase or lipases, electrolytes, creatinine and glucose are frequently

12.8 Approach to Management

13. CHRONIC ABDOMEN / W.G. Thompson

13.3 Causes and Mechanism

13.4 Important Historical Points and Physical Examination Features